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内界膜上水通道蛋白表达增加与糖尿病黄斑水肿的发生的相关性。

The Correlation between the Increased Expression of Aquaporins on the Inner Limiting Membrane and the Occurrence of Diabetic Macular Edema.

机构信息

Center for Rehabilitation Medicine, Department of Ophthalmology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, China.

Department of Retina Center, Affiliated Eye Hospital of Wenzhou Medical University, Hangzhou, 310000 Zhejiang Province, China.

出版信息

Oxid Med Cell Longev. 2022 Apr 28;2022:7412208. doi: 10.1155/2022/7412208. eCollection 2022.

DOI:10.1155/2022/7412208
PMID:35528520
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9071982/
Abstract

PURPOSE

Diabetic macular edema (DME) is a major cause of vision loss in patients with diabetic retinopathy; this study is aimed at comparing the expression of aquaporins (AQPs) on the inner limiting membranes (ILMs) of various vitreoretinal diseases and investigating the role of aquaporins expressed on the ILMs in mediating the occurrence of DME.

METHODS

The whole-mounted ILM specimens surgically excised from patients with various vitreoretinal diseases (idiopathic macular hole, myopic traction maculopathy, and diabetic retinopathy) were analyzed by immunohistochemistry (IHC). The distribution and morphology of AQP4, AQP7, and AQP11 on the ILMs were correlated with immunohistochemical staining characteristics. Moreover, immunofluorescence of AQP4 was performed on the ILM specimens of the patient in four groups: the control group, negative control group, no DME group, and DME group. The immunofluorescence intensity value of AQP4 was measured using ImageJ. The difference between the four groups and the correction between the immunofluorescence value and central foveal thickness (CFT) were analyzed.

RESULTS

In IHC sections, the expression of AQP4, AQP7, and AQP11 on ILMs of diabetic retinopathy (DR) with macular edema, respectively, seemed to be more abundant than in the idiopathic macular hole (iMH) and myopic traction maculopathy (MTM). Moreover, markedly higher fluorescence intensity of AQP4 of ILMs was determined in the DME group (51.05 ± 5.67) versus the other three groups ( < 0.001). A marked positive association was identified between the fluorescence intensity of AQP4 and CFT ( = 0.758; = 0.011).

CONCLUSIONS

AQP4, AQP7, and AQP11 can be expressed on human ILM in vivo. The increased expression of AQPs on the ILMs of DR may be associated with the occurrence of DME. Moreover, the degree of DME may be positively correlated with the expression of AQP4 on the ILMs.

摘要

目的

糖尿病性黄斑水肿(DME)是糖尿病性视网膜病变患者视力丧失的主要原因;本研究旨在比较各种玻璃体视网膜疾病的内界膜(ILM)上水通道蛋白(AQP)的表达,并探讨 ILM 上表达的水通道蛋白在介导 DME 发生中的作用。

方法

通过免疫组织化学(IHC)分析从各种玻璃体视网膜疾病(特发性黄斑裂孔、近视牵引性黄斑病变和糖尿病性视网膜病变)患者手术切除的全贴壁 ILM 标本。AQP4、AQP7 和 AQP11 在 ILM 上的分布和形态与免疫组织化学染色特征相关。此外,对 4 组患者的 ILM 标本进行 AQP4 免疫荧光染色:对照组、阴性对照组、无 DME 组和 DME 组。使用 ImageJ 测量 AQP4 的免疫荧光强度值。分析四组之间的差异以及免疫荧光值与中央凹视网膜厚度(CFT)之间的校正。

结果

在 IHC 切片中,DR 伴黄斑水肿患者的 ILM 上 AQP4、AQP7 和 AQP11 的表达似乎比特发性黄斑裂孔(iMH)和近视牵引性黄斑病变(MTM)更丰富。此外,在 DME 组(51.05±5.67)中确定 ILM 上 AQP4 的荧光强度明显高于其他三组(<0.001)。AQP4 的荧光强度与 CFT 之间存在显著正相关(=0.758;=0.011)。

结论

AQP4、AQP7 和 AQP11 可在人 ILM 中体内表达。DR 患者 ILM 上 AQP 的表达增加可能与 DME 的发生有关。此外,DME 的严重程度可能与 ILM 上 AQP4 的表达呈正相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/d3877f422aaf/OMCL2022-7412208.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/334fc8101542/OMCL2022-7412208.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/63f543e854a9/OMCL2022-7412208.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/42a93ed33690/OMCL2022-7412208.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/106b8c3c0cbe/OMCL2022-7412208.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/50b56036ab9c/OMCL2022-7412208.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/d3877f422aaf/OMCL2022-7412208.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/334fc8101542/OMCL2022-7412208.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/63f543e854a9/OMCL2022-7412208.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/42a93ed33690/OMCL2022-7412208.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/106b8c3c0cbe/OMCL2022-7412208.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/50b56036ab9c/OMCL2022-7412208.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d91c/9071982/d3877f422aaf/OMCL2022-7412208.006.jpg

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